Impact of patatin‐like phospholipase‐3 (rs738409 C>G) polymorphism on fibrosis progression and steatosis in chronic hepatitis C

Eric Trépo, Pierre Pradat, Andrej Potthoff, Yukihide Momozawa, Eric Quertinmont, Thierry Gustot, Arnaud Lemmers, Pascale Berthillon, Leila Amininejad, Michéle Chevallier, Jerome Schlué, Hans Kreipe, Jacques Devière, Michael Manns, Christian Trépo, John Sninsky, Heiner Wedemeyer, Denis Franchimont, Christophe Moreno – 12 April 2011 – Only 20% of patients with chronic hepatitis C (CHC) will develop cirrhosis, and fibrosis progression remains highly unpredictable.

Apoptosis signal‐regulating kinase 1 inhibits hepatocarcinogenesis by controlling the tumor‐suppressing function of stress‐activated mitogen‐activated protein kinase

Hayato Nakagawa, Yoshihiro Hirata, Kohsuke Takeda, Yoku Hayakawa, Takehiro Sato, Hiroto Kinoshita, Kei Sakamoto, Wachiko Nakata, Yohko Hikiba, Masao Omata, Haruhiko Yoshida, Kazuhiko Koike, Hidenori Ichijo, Shin Maeda – 12 April 2011 – The stress‐activated mitogen‐activated protein kinases (MAPKs), c‐Jun NH2‐terminal kinase (JNK), and p38 have been implicated in hepatocarcinogenesis. Although the many interrelated functions of JNK and p38 are precisely regulated by upstream signaling molecules, little is known about upstream regulators.

The metastasis‐associated protein‐1 gene encodes a host permissive factor for schistosomiasis, a leading global cause of inflammation and cancer

Sujit S. Nair, Anitha Bommana, Jeffrey M. Bethony, Amanda J. Lyon, Kazufumi Ohshiro, Suresh B. Pakala, Gabriel Rinaldi, Brian Keegan, Sutas Suttiprapa, Maria V. Periago, Peter J. Hotez, Paul J. Brindley, Rakesh Kumar – 12 April 2011 – Schistosoma haematobium is responsible for two‐thirds of the world's 200 million to 400 million cases of human schistosomiasis. It is a group 1 carcinogen and a leading cause of bladder cancer that occurs after years of chronic inflammation, fibrosis, and hyperproliferation in the host liver.

Fatty acid and endotoxin activate inflammasomes in mouse hepatocytes that release danger signals to stimulate immune cells

Timea Csak, Michal Ganz, Justin Pespisa, Karen Kodys, Angela Dolganiuc, Gyongyi Szabo – 12 April 2011 – The pathogenesis of nonalcoholic steatohepatitis (NASH) and inflammasome activation involves sequential hits. The inflammasome, which cleaves pro–interleukin‐1β (pro–IL‐1β) into secreted IL‐1β, is induced by endogenous and exogenous danger signals. Lipopolysaccharide (LPS), a toll‐like receptor 4 ligand, plays a role in NASH and also activates the inflammasome.

Antiviral activity of the hepatitis C virus polymerase inhibitor filibuvir in genotype 1–infected patients

Frank Wagner, Robert Thompson, Constantino Kantaridis, Paul Simpson, Philip J. F. Troke, Shyla Jagannatha, Srividya Neelakantan, Vivek S. Purohit, Jennifer L. Hammond – 12 April 2011 – More effective and better‐tolerated therapies are needed for chronic hepatitis C virus (HCV) infection. Among the direct‐acting anti‐HCV agents in development is the nonstructural 5B protein (NS5B polymerase) non‐nucleoside inhibitor filibuvir.

Serum and liver iron differently regulate the bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway in mice

Elena Corradini, Delphine Meynard, Qifang Wu, Shan Chen, Paolo Ventura, Antonello Pietrangelo, Jodie L. Babitt – 12 April 2011 – The bone morphogenetic protein 6 (BMP6)‐SMAD signaling pathway is a central regulator of hepcidin expression and systemic iron balance. However, the molecular mechanisms by which iron is sensed to regulate BMP6‐SMAD signaling and hepcidin expression are unknown. Here we examined the effects of circulating and tissue iron on Bmp6‐Smad pathway activation and hepcidin expression in vivo after acute and chronic enteral iron administration in mice.

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